Neuromuscular Science Ch. 8 Study Guide

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tap is also influenced by spindle sensitivity which leads to↓ spindle sensitivity with stretching

• MEP (motor evoked potentials) not affected until large stretch imposed

o α-MN excitability not affected until large stretch imposed

14. What occurs as a result of small vs. large stretches?

• Small stretch leads to reduction in size of reflexes due to Ia pre-synaptic inhibition

• Large stretch leads to ↓ excitability of α-MN pool (postsynaptic inputs, eg Ib input) contributes to depression of reflexes as the stretch increases

15. ___Autogenic inhibition____________ inhibition is occurring during contract-relax PNF stretching.

16. ___Reciprocal inhibition____________ inhibition is occurring antagonist-contract PNF stretching.

17. Why do PNF stretching techniques allow for greater increases in joint range of motion in comparison to static stretching?

PNF techniques affect H-reflex more than static stretching, which is why PNF allows greater acute increases in ROM.

18. When does delayed onset muscle soreness start after an exercise bout?

Soreness starts 24-48 hours following exercise bout.

19. What are some clinical indices (i.e., markers of change in muscle and blood plasma) that would be present in a person with delayed onset muscle soreness?

• Creatine kinase (CK, aka CPK), myoglobin, and other muscle proteins present in plasma

• Ultrastructural damage of muscle

• Decreased muscle performance

• “tenderness to applied pressure”

20. What contraction (concentric or eccentric) type promotes the greatest degree of muscle damage and soreness?

Eccentric

21. Are individuals that are “unaccustomed” to a particular type of exercise more or less likely to experience delayed onset muscle soreness when compared to a person who is more highly trained?

The unaccustomed individuals are more likely to experience delayed onset muscle soreness compare to a highly trained person.

22. What two models have been proposed to explain the cause of muscle soreness? Describe/define each model.

• Signaling theory: altered excitation-contraction coupling leads to ↑ intracellular [Ca++].

o Altered signaling of T-tubule and sarcoplasmic reticulum receptors (ryanodine and dihydropyridine)

o Altered E-C coupling leads to strength loss

• Mechanical theory: mechanical damage to muscle fibers

o Contraction preferentially damages sarcomeres with less actin-myosin overlap → damaged sarcomeres lead to further damage of other sarcomeres with repeated contractions → damage to sarcoplasmic reticulum, t-tubule, and sarcolemma → loss of Ca++ homeostasis → Ca++ mediated damage

23. What is the effect of delayed onset muscle soreness on muscle strength?

DOMS is associated with muscle weakness so it will decrease in muscle strength.

24. Describe the effects of delayed onset muscle soreness on voluntary activation and maximal voluntary contraction (MVC). Remember: Voluntary activation = descending neural drive, or a measure of the extent to which the nervous system can elicit the maximal force a muscle can produce.

• Voluntary activation

o 97% at 2 hours post DOMS-inducing exercise

o 90% at 24 hours

o Back to control level at 8 days

• MVC torque

o Still depressed by ~25% at day 8

25. Does delayed onset muscle soreness have a more deleterious effect on voluntary activation or MVC? What is muscle weakness associated with following an exercise bout that induces delayed onset muscle soreness?

It has more effect on the MVC torque because even by day 8 it is still depressed by 25% while the voluntary activation is back to control levels.

26. Describe the effects of DOMS on Lo and the level of passive tension at Lo.

• Length of optimal force output (Lo) changes with DOMS

o Consistent with muscle mechanical damage model, the length at which a muscle fiber or whole muscle produces its peak force increases after a bout of lengthening contractions.

27. What is the “repeated bout” effect in the context of DOMS?

Repeated-bout effect is due to the addition of new sarcomeres to the damaged myofibrils so that subsequent lengthening contractions are less likely to stretch sarcomeres to a length that damages them. So previous exposure to DOMS-inducing exercise decreases extent of DOMS symptoms on subsequent exposure.